Actualización en COVID-19 y enfermedad hepática

Téllez, Luís; Mateos, Rosa María Martín

doi:10.1016/j.gastrohep.2020.06.006

Cited by 30 publications

(17 citation statements)

References 50 publications

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“…Frequent additional factors associated with elevated liver injury indicators were decreased lymphocyte count, increased neutrophil count, and male gender. 5 , 22 …”

Section: Discussionmentioning

confidence: 99%

Impact of liver enzymes on SARS-CoV-2 infection and the severity of clinical course of COVID-19

et al. 2021

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“…Frequent additional factors associated with elevated liver injury indicators were decreased lymphocyte count, increased neutrophil count, and male gender. 5 , 22 …”

Section: Discussionmentioning

confidence: 99%

Impact of liver enzymes on SARS-CoV-2 infection and the severity of clinical course of COVID-19

et al. 2021

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“…106 Likely, the presence of already activated inflammatory pathways in patients with MAFLD is associated with more severe SIRS development when they are infected with SARS-CoV-2. 107 The increased ACE2 expression on hepatocytes of patients with MAFLD 108 and paired hepatic innate immune system in these patients are potential mechanisms that would explain the increased risk of severe COVID-19 in patients with MAFLD. 109 Autoimmune liver disease, treated with immunomodulatory or immunosuppressive drugs, could increase the risk of complications associated with COVID-19.…”

Section: Liver Damage In Pre-existing Liver Diseasementioning

confidence: 99%

COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence

Idalsoaga¹,

Ayares²,

Arab³

et al. 2021

Journal of Clinical and Translational Hepatology

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The liver is frequently affected by severe acute respiratory syndrome-coronavirus 2 (SARS-CoV-2) infection. The most common manifestations are mildly elevated alanine aminotransferase and aspartate aminotransferase, with a prevalence of 16-53% among patients. Cases with severe coronavirus disease 2019 (COVID-19) seem to have higher rates of acute liver dysfunction, and the presence of abnormal liver tests at admission signifies a higher risk of severe disease during hospitalization. Patients with chronic liver diseases also have a higher risk of severe disease and mortality (mainly seen in patients with metabolic-associated fatty liver disease). Several pathways of damage have been proposed in the liver involvement of COVID-19 patients; although, the end-cause is most likely multifactorial. Abnormal liver tests have been attributed to the expression of angiotensin-converting enzyme 2 receptors in SARS-CoV-2 infection. This enzyme is expressed widely in cholangiocytes and less in hepatocytes. Other factors attributed to liver damage include drug-induced liver injury, uncontrolled release of proinflammatory molecules ("cytokine storm"), pneumonia-associated hypoxia, and direct damage by the infection. Hepatic steatosis, vascular thrombosis, fibrosis, and inflammatory features (including Kupffer cell hyperplasia) are the most common liver histopathological findings in deceased COVID-19 patients, suggesting important indirect mechanisms of liver damage. In this translational medicinebased narrative review, we summarize the current data on the possible indirect mechanisms involved in liver damage due to COVID-19, the histopathological findings, and the impact of these mechanisms in patients with chronic liver disease.

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“…The exact mechanism of this liver injury in the context of COVID-19 infection is not completely understood, but a few factors have been postulated to play a role. One mechanism is direct damage from viral replication within cells [5,7,8]. Based on prior studies of the coronavirus family, it has been demonstrated that the virus enters cells via the ACE2 receptor, which is expressed on multiple cells in the body including hepatocytes and bile duct epithelial cells [6,8].…”

Section: Introductionmentioning

confidence: 99%

“…One mechanism is direct damage from viral replication within cells [5,7,8]. Based on prior studies of the coronavirus family, it has been demonstrated that the virus enters cells via the ACE2 receptor, which is expressed on multiple cells in the body including hepatocytes and bile duct epithelial cells [6,8]. Viral replication and release result in the rupture of cells, generating elevated liver enzymes in the serum [8].…”

Section: Introductionmentioning

confidence: 99%

COVID-19 Presenting as Acute Icteric Hepatitis

Balaja¹,

Jacob²,

Hamidpour³

et al. 2021

Cureus

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As the coronavirus pandemic continues to evolve, so does the understanding of different presentations of disease. In this case report, we describe a patient whose presentation of COVID-19 was with acute icteric hepatitis without respiratory symptoms. This is the first case in the literature to our knowledge to report jaundice as the initial presentation of disease and adds to just a handful of cases in the literature of acute hepatitis as the sole presentation of COVID-19. Additionally, despite severe hepatitis, the patient had a benign course of COVID-19 and did not require aggressive medical care; this strays from conventional paradigms that associate severity of COVID-19 with a degree of aminotransferase elevation. The purpose of this report is to make physicians aware of acute icteric hepatitis as a presentation of COVID-19 infection and to facilitate discussion and further research in the area of COVID-19-induced hepatitis.

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Actualización en COVID-19 y enfermedad hepática

Cited by 30 publications

References 50 publications

Impact of liver enzymes on SARS-CoV-2 infection and the severity of clinical course of COVID-19

Impact of liver enzymes on SARS-CoV-2 infection and the severity of clinical course of COVID-19

COVID-19 and Indirect Liver Injury: A Narrative Synthesis of the Evidence

COVID-19 Presenting as Acute Icteric Hepatitis

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